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dc.contributor.authorBregagnollo, Edson A.
dc.contributor.authorZornoff, Leonardo Antonio Mamede [UNESP]
dc.contributor.authorOkoshi, Katashi [UNESP]
dc.contributor.authorSugizaki, Mario
dc.contributor.authorMestrinel, Marco A.
dc.contributor.authorPadovani, Carlos Roberto [UNESP]
dc.contributor.authorCicogna, Antonio Carlos [UNESP]
dc.date.accessioned2014-05-20T13:32:52Z
dc.date.available2014-05-20T13:32:52Z
dc.date.issued2007-04-12
dc.identifierhttp://dx.doi.org/10.1016/j.ijcard.2006.06.006
dc.identifier.citationInternational Journal of Cardiology. Clare: Elsevier B.V., v. 117, n. 1, p. 109-114, 2007.
dc.identifier.issn0167-5273
dc.identifier.urihttp://hdl.handle.net/11449/11225
dc.description.abstractObjectives: To analyze the potential contribution of contractility state and ventricular geometry to the development of heart failure in rats with aortic stenosis.Methods: Rats were divided into three groups: compensated aortic stenosis (AS, n = 11), heart failure AS (n = 12) and control rats (C, n = 13).Results: After 21 weeks, failing AS rats presented higher systolic (C = 36.6 +/- 3.1, AS-78.6 +/- 4.8*, failing AS = 104.6 +/- 7.8*) and diastolic meridian stress (C = 6.9 +/- 0.4, AS = 20.1 +/- 1.1*, failing AS = 43.2 +/- 3.2*(dagger)), hydroxyproline (C = 3.6 +/- 0.7 mg/g, AS = 6.6 +/- 0.6* mg/g, failing AS = 9.2 +/- 1.4*(dagger) mg/g) and cross-sectional area (C = 338 +/- 25 mu m(2), AS = 451 +/- 32* mu m(2), failing AS = 508 +/- 36*(dagger) mu m(2)), in comparison with control and compensated AS animals (*p < 0.05 vs. control, (dagger)p < 0.05 vs. AS). In the isometric contraction study, considering the time from peak tension to 50% relaxation (RT50), the relative variation responses, following post-rest contraction and increase in Ca2+ concentration, were higher in failing AS than compensated AS animals. In contrast, following post-rest contraction, compensated AS group presented higher values of the peak developed tension (DT) than failing AS group. Following beta-adrenergic stimulation, control animals presented higher values of +dT/dt and -dT/dt than AS animals. In addition, failing AS animals presented higher TPT values than compensated AS animals.Conclusion: Myocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosis. (c) 2006 Elsevier B.V.. All rights reserved.en
dc.format.extent109-114
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofInternational Journal of Cardiology
dc.sourceWeb of Science
dc.subjectcardiac dysfunctionpt
dc.subjectfibrosispt
dc.subjecthypertrophypt
dc.subjectpressure overloadpt
dc.subjectventricular remodelingpt
dc.titleMyocardial contractile dysfunction contributes to the development of heart failure in rats with aortic stenosisen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.description.affiliationUniv Estadual Paulista, Fac Med Botucantu, Dept Clin Med, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUniv Estadual Paulista, Inst Biociencias, Dept Bioestarist, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Fac Med Botucantu, Dept Clin Med, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Inst Biociencias, Dept Bioestarist, BR-18618000 Botucatu, SP, Brazil
dc.identifier.doi10.1016/j.ijcard.2006.06.006
dc.identifier.wosWOS:000245839200016
dc.rights.accessRightsAcesso restrito
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
dc.identifier.lattes1590971576309420
dc.identifier.lattes9418970103564137
dc.identifier.lattes5016839015394547
unesp.author.lattes5016839015394547[2]
unesp.author.lattes1590971576309420
unesp.author.lattes9418970103564137[7]
unesp.author.lattes8727897080522289[6]
unesp.author.orcid0000-0002-4402-6523[7]
unesp.author.orcid0000-0002-7719-9682[6]
dc.relation.ispartofjcr4.034
dc.relation.ispartofsjr1,200
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